Unlike Sun1−/−Sun2−/− or Syne1−/−Syne2−/− mice, which suffer from defective neocortical lamination and fail to thrive after birth (Zhang et al., 2009), the viable Sun1−/− and Sun−/−Sun2+/− animals, which present with cerebellar ataxia, might serve as a working model for the study of the molecular mechanisms underlying SYNE1-associated ARCA1 (Dupré et al., 2007; Gros-Louis et al., 2007), as well as for the identification of therapeutic targets in neurodegenerative diseases involving Purkinje cell loss (Millen and Gleeson, 2008). The gene discussed is SYNE1; the disease is cerebellar ataxia.